Co-infection with opportunistic pathogens promotes human immunodeficiency virus type 1 infection in macrophages

Human immunodeficiency virus type 1 (HIV-1) infection is dependent on susce ptible host cells that express both CD4 and chemokine co-receptors. The co- receptor CCR5 is associated with primary infection by macrophage-tropic vir us isolates, whereas CXCR4 is commonly associated with T cell- and dual-tro pic viruses. Once infected, lymphocytes and macrophages may replicate HIV-1 or harbor latent virus, depending on environmental factors and cellular ac tivation. Immune activation is often associated with viremia, which is cons istent with enhanced infection and viral replication in activated cells har boring virus. In this regard, opportunistic infections activate the immune system with the detrimental sequelae of enhanced viral replication and vire mia. Under these conditions, viral expansion extends beyond T cells to tiss ue macrophages, many of which are co-infected with opportunistic pathogens. The opportunistic infections promote macrophage susceptibility to HIV-1 th rough cytokine modulation and altered chemokine co-receptors, potential tar gets for intervention.